New potential drug blocks all HIV strains, raises hope for vaccine

In a remarkable new advance against the virus that causes AIDS, scientists from The Scripps Research Institute (TSRI), California have announced the creation of a novel drug candidate that is so potent and universally effective, it might work as part of an unconventional vaccine.

In a remarkable new advance against the virus that causes AIDS, scientists from The Scripps Research Institute (TSRI), California have announced the creation of a novel drug candidate that is so potent and universally effective, it might work as part of an unconventional vaccine.

The research, which involved scientists from more than a dozen research institutions and both campuses of TSRI, was published February 18 online ahead of print by the journal Nature.

The study shows that the new drug candidate blocks every strain of HIV-1, HIV-2 and SIV (simian immunodeficiency virus) that has been isolated from humans or rhesus macaques, including the hardest-to-stop variants. It also protects against much-higher doses of virus than occur in most human transmission and does so for at least eight months after injection.

“Our compound is the broadest and most potent entry inhibitor described so far,” said Michael Farzan, a professor on TSRI's Florida campus who led the effort. “Unlike antibodies, which fail to neutralize a large fraction of HIV-1 strains, our protein has been effective against all strains tested, raising the possibility it could offer an effective HIV vaccine alternative.”

When HIV infects a cell, it targets the CD4 lymphocyte, an integral part of the body’s immune system. HIV fuses with the cell and inserts its own genetic material—in this case, single-stranded RNA—and transforms the host cell into a HIV manufacturing site.

The new study builds on previous discoveries by the Farzan laboratory, which show that a co-receptor called CCR5 contains unusual modifications in its critical HIV-binding region, and that proteins based on this region can be used to prevent infection.

“This is the culmination of more than a decade’s worth of work on the biochemistry of how HIV enters cells,” Farzan said. “When we did our original work on CCR5, people thought it was interesting, but no one saw the therapeutic potential. That potential is starting to be realized.”